Alzheimer's disease (AD) deaths have increased by 89% since 2000. This alarming trajectory of neurological disease highlights the failure of current best practice. Deteriorating brain fuel supply is the nemesis of intact neurological health. Cerebral hypo-metabolism associated with AD occurs years before onset. Both the
ketogenic diet and calorie restriction (fasting) lead to a compensatory rise in
ketones to improve energy deficits in the brain derived from cerebral
insulin resistance. Two forms of
ketone bodies, β-hydroxybutyrate and
acetoacetate, fuel the brain during
starvation, fasting and strenuous exercise.
Ketones are
neuroprotective agents that shelter the aging brain from
memory loss and neurodegeneration. Induced
ketone production has been shown to ameliorate mitochondrial function, reduce the expression of apoptotic and inflammatory mediators and provide neuroprotection to cells (Lange et al., 2017). This case study highlights an innovative research design aimed at attenuating memory decline in a 57 year old female previously diagnosed with comorbid
mild cognitive impairment (MCI) and
metabolic syndrome (MetS).
Mild cognitive impairment is a predementia syndrome known to precede AD (Michaud et al, 2017). The 12-week intervention included ketogenic nutrition protocol, high intensity interval training (HIIT) and
memory training using the PEAK
brain training app. Memory function was assessed via the MoCA (Montreal Cognitive Assessment) pre/post intervention. Physiological
biomarkers for MetS including HOMA-IR(homeostatic model assessment of
insulin resistance),
triglyceride/HDL ratio, HgA1c, fasting
triglycerides and HDL were measured pre/post intervention. MoCA baseline score was 22/30 (MCI); post intervention score: 30/30 (normal). MetS
biomarker improvements also reflected statistical significance.